Summary

In a study of the role of sex and iodine deficiency in the growth and function of thyroid carcinoma in rats, half of the male and female litter rats were surgically gonadectomized at the age of two months. One month later, all animals were implanted with a transplantable, autonomous, follicular thyroid carcinoma and one-half of all animals were given an iodine-deficient diet. Six weeks later, the animals were injected with 131I and thymidine-3H and sacrificed.

The tumor was derived from the male rat thyroid gland by transplantation in the male, inbred isologous rat. In castrated male, iodine-deficient rats the tumor grew faster (greater tumor weight, thymidine-3H-DNA specific activity, and cell nuclei labeling) than in castrated male rats on the regular diet and in normal male rats on the regular or iodine-deficient diet. The growth of the tumor in all female rats was several times slower and was not affected by diet and/or gonadectomy.

The tumor 131I uptake was higher in normal rats of both sexes on an iodine-deficient diet than in any other rats. When expressed per unit of weight of tissue, the tumor 131I uptake was equal in the male and female rats. The tumor 131I uptake was decreased by gonadectomy possibly as a consequence of an associated decrease in thyrotropin secretion.

The dominant factor in increased tumor growth was a lack of testicular hormones combined with an increased secretion of thyrotropin (resulting from iodine deficiency). Each separately contributed little to the growth of the tumor. The enlarged and presumably overactive adrenals could have influenced the tumor growth in the castrated male iodine-deficient host. The immune response of the female host to the male Y-chromosome of the tumor may have had an adverse effect on the tumor growth.

Footnotes

↵1 Supported by funds from the Michigan Cancer Foundation Grant-in-Aid No. A67-154A and from the USPHS CA-06381.